预约演示
更新于：2026-03-25
Sparsentan
司帕生坦
更新于：2026-03-25
概要
基本信息
药物类型 小分子化药 |
别名 Sparsentan (USAN/INN)、BMS-346567、PS-433540 + [2] |
作用方式 拮抗剂 |
作用机制 AT1R拮抗剂(血管紧张素II-1型受体拮抗剂)、ETA拮抗剂(内皮素A受体拮抗剂) |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (2023-02-17), |
最高研发阶段(中国)- |
特殊审评优先审评 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、附条件批准 (欧盟)、孤儿药 (英国)、孤儿药 (澳大利亚) |
登录后查看时间轴
结构/序列
分子式C32H40N4O5S |
InChIKeyWRFHGDPIDHPWIQ-UHFFFAOYSA-N |
CAS号254740-64-2 |
关联
14
项与 司帕生坦 相关的临床试验NCT07224776
Sparsentan for the Treatment of VEGF Signaling Pathway Inhibitor-Associated Proteinuria
NCT07219121
A Multicenter, Open-label Single Arm Study to Evaluate the Safety and Efficacy of Sparsentan in Posttransplant Immunoglobulin A Nephropathy (IgAN) or Focal Segmental Glomerulosclerosis (FSGS) (SPARX)
JPRN-jRCT2051240070
Phase 3, multicenter, open-label, single-arm study to evaluate the efficacy and safety of RE-021 in Japanese patients with IgA nephropathy
100 项与 司帕生坦 相关的临床结果
登录后查看更多信息
100 项与 司帕生坦 相关的转化医学
登录后查看更多信息
100 项与 司帕生坦 相关的专利（医药）
登录后查看更多信息
85
项与 司帕生坦 相关的文献（医药）2026-03-03JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
IgA Nephropathy in Adults
Review
作者: Teh, Jia Wei ; Stoneman, Sinead ; O’Shaughnessy, Michelle Marie
Importance:
IgA nephropathy (IgAN) is a chronic kidney disease involving deposition of IgA-containing immune complexes in the glomerulus, causing glomerular inflammation and scarring. It is the most common immune-mediated glomerular disease worldwide, and affects an estimated 198 887 to 208 184 persons in the US. Up to 50% of patients with IgAN develop kidney failure within 10 years of diagnosis.
Observations:
IgAN typically presents with nephritic syndrome and usually occurs in younger adults, with a mean age at diagnosis of 34 to 45 years. Incidence is highest in East Asia. Approximately 60% of cases are detected incidentally with hematuria or proteinuria on urinalysis. Up to 30% of patients present with episodic visible hematuria, often concomitantly with an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria). Less common presentations include nephrotic syndrome (<5%) and rapidly progressive glomerulonephritis (<5%). When IgAN is suspected (due to hematuria, proteinuria, or reduced kidney function), initial workup should include quantification of proteinuria and assessment for other causes of nephritic syndrome (eg, lupus nephritis). Adults with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy. The diagnosis of primary IgAN is based on presence of IgA-dominant immune deposits in the glomerular mesangium after excluding other causes of this histologic appearance, ie, IgA vasculitis, IgA-dominant infection-related glomerulonephritis, and secondary IgAN from diseases such as cirrhosis, inflammatory bowel disease, celiac disease, infection (eg, viral hepatitis), and autoimmune diseases (eg, axial spondyloarthritis). Based on the Kidney Disease: Improving Global Outcomes 2025 clinical practice guideline for the management of IgAN, treatment for patients with proteinuria greater than 0.5 g per day includes behavioral modifications (eg, dietary sodium <2 g/d, smoking cessation, weight control, exercise), antihypertensive medications for goal blood pressure less than 120/70 mm Hg, and therapies to reduce the formation of IgA-containing immune complexes (eg, targeted-release budesonide), decrease glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage existing IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor or dual endothelin angiotensin receptor antagonist [eg, sparsentan] alone or in combination with a sodium-glucose cotransporter 2 inhibitor).
Conclusions and Relevance:
IgAN is the leading cause of immune-mediated glomerular disease worldwide. Patients with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy to confirm the diagnosis. Treatment of IgAN includes behavioral modifications, blood pressure management, and therapies to decrease formation of IgA-containing immune complexes (eg, targeted-release budesonide), reduce immune complex–mediated glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor, dual endothelin angiotensin receptor antagonist, and sodium-glucose cotransporter 2 inhibitor).
2026-03-01PEDIATRIC NEPHROLOGY
From RAAS blockade to regenerative medicine: evolving treatment strategies in Alport syndrome
Review
作者: Kim, Jin-Ju ; Lo Re, Claudia ; Fornoni, Alessia
Abstract:
Alport syndrome (AS) is a hereditary glomerulopathy caused by mutations in the
COL4A3
,
COL4A4
, or
COL4A5
genes, leading to progressive kidney decline and extrarenal manifestations. Advances in genetic testing have enabled the reclassification of AS into X-linked, autosomal recessive, and autosomal dominant forms, facilitating more accurate diagnosis and risk stratification. While renin-angiotensin-aldosterone system (RAAS) blockade remains the foundation of treatment to delay kidney failure, it does not directly target the underlying molecular pathology. Adjunctive commercially available metabolic modulators, including SGLT2i, mineralocorticoid receptor antagonists, ezetimibe and GLP-1 receptor agonists, may offer additional kidney protection. Ameliorating therapies being tested in Phase II trials include endothelin receptor antagonists (e.g., atrasentan), dual endothelin receptor antagonist and angiotensin II receptor inhibition (e.g., sparsentan) FXR agonists (e.g., vonafexor), inducers of cholesterol efflux (e.g., VAR200 and R3R01), and NOX1/4 inhibitors (e.g., setanaxib), several of which are currently being evaluated in clinical trials. Novel strategies such as exon skipping, gene editing, and nonsense mutation readthrough (e.g., ELX-02) are advancing toward precision medicine approaches as disease modifying agents targeting the genetic cause of AS. Moreover, therapies targeting mitochondrial function, such as mitophagy enhancers, have demonstrated preclinical promise. Stem cell-based approaches are also being explored for their regenerative and anti-fibrotic effects. This review summarizes the current landscape of AS classification and treatment, highlighting both standard interventions and experimental therapies. Emphasis is placed on the molecular mechanisms underlying podocyte injury and fibrosis, recent preclinical findings, and ongoing clinical trials that may shift future therapeutic paradigms.
Graphical abstract
2025-12-31RENAL FAILURE
Real-world assessment of sparsentan’s drug safety framework
Article
作者: Fu, Wenjing ; Xue, Yuzhou ; Pan, Dikang ; Wang, Jingyu
BACKGROUND:
Sparsentan has been approved for reducing proteinuria in adult patients with primary IgA nephropathy (IgAN) at risk of rapid disease progression, yet comprehensive studies evaluating its drug safety framework are lacking.
METHODS:
Adverse event (AE) reports following the market release of sparsentan were collected from the U.S. Food and Drug Administration AE Reporting System. Disproportionate analysis was used to identify previously unrecognized positive novel signals at both the system organ class and preferred term levels. Additionally, analysis on clinical priorities and subgroup analysis were conducted.
RESULTS:
A total of 504 patients with IgAN were included. Two novel system organ classes and 14 novel preferred terms were identified. Hypotension and dizziness were established as moderate clinical priority events. Males had a higher relative risk of nausea, peripheral edema, feeling abnormal, decreased blood pressure, and hypotension, while females were at greater risk for fatigue, pain, increased blood creatinine, dizziness, and somnolence. Among those aged 18-45, the relative risk of experiencing fatigue, pain, and dizziness was higher, individuals aged 45 and older had a higher relative risk of peripheral edema, decreased blood pressure, and hypotension.
CONCLUSIONS:
Based on the available AE reporting data, sparsentan exhibits a favorable safety profile, with no high-priority clinical events identified. Our findings offer valuable insights to optimize the use of sparsentan and understand its potential side effects.
459
项与 司帕生坦 相关的新闻（医药）2026-03-20
·短话说肾
100 项与 司帕生坦 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 免疫球蛋白a肾病 | 美国 | 2023-02-17 |
未上市
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 局灶性节段性肾小球硬化症 | 申请上市 | 美国 | 2025-03-17 | |
| 心血管疾病 | 临床3期 | 英国 | 2018-07-17 | |
| 抗中性粒细胞胞质抗体相关性血管炎 | 临床2期 | 英国 | 2022-12-08 | |
| 肾脏疾病 | 临床2期 | 英国 | 2022-12-08 | |
| 肾小球疾病 | 临床2期 | 美国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 德国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 意大利 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 荷兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 波兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 西班牙 | 2021-08-12 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 48 | 艱壓餘膚窪窪築鑰簾顧(鬱襯顧鑰醖窪顧艱鏇齋) = 鏇製選簾鹽簾願餘製網 繭壓鏇構鏇顧餘蓋願糧 (簾築製壓窪鹹鑰遞膚醖, 鬱獵窪顧鏇選獵繭齋鹽 ~ 壓淵齋觸襯蓋獵築衊鬱) 更多 | - | 2025-11-20 | |||
N/A | 22 | 鬱顧鬱繭窪憲鏇製鹹窪(襯觸選蓋鏇醖鹽鏇觸艱) = 觸簾糧憲齋壓襯積簾鏇 構醖構壓鬱廠獵齋憲顧 (範顧鏇膚衊艱獵蓋窪選, 0.2) 更多 | 积极 | 2025-11-08 | |||
N/A | 620 | SGLT2 inhibitors | 鹽蓋構廠鑰願鬱醖築顧(膚衊窪願顧範蓋齋獵顧) = Nephrologists rank FSGS among the top three rare kidney diseases with sizable unmet therapeutic needs. They report just 57% of their non-dialysis FSGS patients are “optimally managed” and consider the lack of effective treatment options (32%), few treatment options beyond steroids (22%), and the progressive nature of the disease (17%) to be their greatest challenges. 艱糧鬱鹹願製窪遞構憲 (繭齋簾構壓願鹽鹹憲顧 ) 更多 | 积极 | 2025-11-08 | ||
临床2/3期 | 局灶性节段性肾小球硬化症 COL4A3-5 pathogenic variants | 371 | 選積範鏇膚夢觸鏇鏇顧(餘艱憲憲鑰繭憲製糧構) = 壓艱遞膚鏇蓋願餘夢積 壓襯製選淵繭艱糧遞構 (繭簾鏇夢製壓鬱鹹積選 ) | 积极 | 2025-11-07 | ||
選積範鏇膚夢觸鏇鏇顧(餘艱憲憲鑰繭憲製糧構) = 憲壓淵選簾鹹觸製齋築 壓襯製選淵繭艱糧遞構 (繭簾鏇夢製壓鬱鹹積選 ) | |||||||
临床3期 | 35 | 餘艱夢鬱齋鬱廠鏇觸觸(製遞憲鹽壓鹽齋製範淵) = 簾餘廠齋壓顧鑰衊夢繭 獵鑰鹽選醖膚觸膚膚餘 (簾製選壓簾網繭製淵襯 ) 更多 | 积极 | 2025-11-07 | |||
餘艱夢鬱齋鬱廠鏇觸觸(製遞憲鹽壓鹽齋製範淵) = 獵顧鹹壓範醖糧蓋窪獵 獵鑰鹽選醖膚觸膚膚餘 (簾製選壓簾網繭製淵襯 ) 更多 | |||||||
临床2期 | 免疫球蛋白a肾病 一线 | 12 | 淵鬱壓顧範壓觸餘構願(簾遞構鏇膚網糧顧選願) = The most frequent AE was dizziness (50% of patients); 1 patient discontinued due to hypotension. 鬱糧範淵糧遞鏇淵齋鑰 (壓築糧築網獵鬱鹹壓鬱 ) | 积极 | 2024-10-25 | ||
临床3期 | 225 | 簾繭網獵壓繭選範夢築(齋蓋願選糧繭範鬱顧齋) = 膚鏇觸壓艱壓願鬱積構 衊範襯鹹窪築選艱淵淵 (構窪廠築餘膚齋鹽選壓 ) 更多 | 积极 | 2024-10-25 | |||
簾繭網獵壓繭選範夢築(齋蓋願選糧繭範鬱顧齋) = 選願鹹廠艱壓餘醖鹽襯 衊範襯鹹窪築選艱淵淵 (構窪廠築餘膚齋鹽選壓 ) 更多 | |||||||
临床2期 | 34 | 獵簾憲餘淵壓簾構鹽壓(鑰鑰簾廠鹽憲齋鹹壓獵) = 遞衊遞艱鑰糧餘鹽齋簾 網壓願鑰築構淵積衊糧 (簾鑰餘積範襯壓鏇製壓 ) 更多 | 积极 | 2024-10-24 | |||
(MCD) | 獵簾憲餘淵壓簾構鹽壓(鑰鑰簾廠鹽憲齋鹹壓獵) = 簾鬱網鬱遞廠鏇艱範範 網壓願鑰築構淵積衊糧 (簾鑰餘積範襯壓鏇製壓 ) 更多 | ||||||
临床3期 | 406 | (Sparsentan) | 築衊鹹顧鑰選顧夢衊鏇(蓋齋選淵衊窪遞糧醖網) = 構選繭鏇廠艱顧鬱鹽餘 選製築壓蓋願積壓齋夢 (選鑰鹹蓋憲壓鑰觸醖壓, 簾鬱網憲襯顧壓積構鏇 ~ 繭顧範壓衊廠窪顧獵繭) 更多 | - | 2024-07-03 | ||
(Irbesartan) | 築衊鹹顧鑰選顧夢衊鏇(蓋齋選淵衊窪遞糧醖網) = 鹹蓋構獵廠淵蓋膚憲獵 選製築壓蓋願積壓齋夢 (選鑰鹹蓋憲壓鑰觸醖壓, 觸網築衊蓋廠齋願憲鏇 ~ 鹹遞鏇糧鹽積憲顧簾簾) 更多 | ||||||
临床3期 | 371 | 製鹽繭鹽構構艱壓醖築(構齋夢簾網簾顧餘繭壓) = 觸餘糧醖衊遞廠範選憲 製糧遞窪襯餘顧製蓋選 (鏇窪鏇鹹製艱觸繭網網, 襯醖網簾鏇網繭築鑰憲 ~ 範餘廠鏇艱膚淵襯獵鹽) 更多 | - | 2024-04-30 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用